2011
DOI: 10.1590/s0100-879x2011007500008
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Angiotensin II induces NF-κB, JNK and p38 MAPK activation in monocytic cells and increases matrix metalloproteinase-9 expression in a PKC- andRho kinase-dependent manner

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Cited by 16 publications
(13 citation statements)
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References 27 publications
(23 reference statements)
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“…In fact the antiinflammatory effects of DIZE in most recent studies 43,46 may also involve the ACE2/Ang-(1-7)/Mas axis, since Ang IImediated signaling is known to activate MAPK and the NF-jB signaling pathway. 47,48 Nevertheless, since DIZE is a small molecular compound and has been used as a drug for the treatment of trypanosomiasis and babesiosis. 49 Possible offtargets effects unrelated to the renin-angiotensin system cannot be ruled out and future studies should be conducted for further understanding of the underlying mechanisms.…”
Section: Discussionmentioning
confidence: 99%
“…In fact the antiinflammatory effects of DIZE in most recent studies 43,46 may also involve the ACE2/Ang-(1-7)/Mas axis, since Ang IImediated signaling is known to activate MAPK and the NF-jB signaling pathway. 47,48 Nevertheless, since DIZE is a small molecular compound and has been used as a drug for the treatment of trypanosomiasis and babesiosis. 49 Possible offtargets effects unrelated to the renin-angiotensin system cannot be ruled out and future studies should be conducted for further understanding of the underlying mechanisms.…”
Section: Discussionmentioning
confidence: 99%
“…Phospholipase A2 activity is a crucial enzyme in the regulation of the production and release of prostaglandin, which induces myometrium contraction and cervix ripening [29,30]. Moreover, Nmbr stimulation also results in activation of tyrosine kinases and tyrosine phosphorylation of p125FAK by a phospholipase C-independent mechanism which requires p21 and the integrity of the actin cytoskeleton [31]. Nmbr activation also stimulates tyrosine phosphorylation of paxillin and MAP kinase activation [32].…”
Section: Zhang Et Almentioning
confidence: 99%
“…17,18 In our study; Losartan pretreatment in animal model of I/Rat a dose of 20 mg/kg/day for 6 weeks before induction of I/R achieved a biochemical cardioprotective effect through reduction of I/R induced elevation of IL-6, TNF-α and CRP. Angiotensin II is described as a potent pro-inflammatory mediator causing up regulation of macrophages to induce inflam- 19 Furthermore, angiotensin II has been found to have a dual effect on macrophages through activation of the mitogenactivated protein kinase (MAPK) pathway and up-regulation of early growth response-1 (Egr-1) gene expression which both master the switch for vascular inflammatory responses. 20,21 So, by blocking Ang II signaling, Losartan reduces the inflammatory response as presented in different studies concerned with heart failure treatment outcomes [22][23][24] Losartan induced elevation of NO level in the animal model could reflect the ability of this drug to improve endothelial functions.…”
Section: Discussionmentioning
confidence: 99%